Last data update: May 13, 2024. (Total: 46773 publications since 2009)
Records 1-2 (of 2 Records) |
Query Trace: Keene KM[original query] |
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Virulence variation among isolates of western equine encephalitis virus in an outbred mouse model
Logue CH , Bosio CF , Welte T , Keene KM , Ledermann JP , Phillips A , Sheahan BJ , Pierro DJ , Marlenee N , Brault AC , Bosio CM , Singh AJ , Powers AM , Olson KE . J Gen Virol 2009 90 1848-58 Little is known about viral determinants of virulence associated with western equine encephalitis virus (WEEV). Here, we have analysed six North American WEEV isolates in an outbred CD1 mouse model. Full genome sequence analyses showed < or =2.7 % divergence among the six WEEV isolates. However, the percentage mortality and mean time to death (MTD) varied significantly when mice received subcutaneous injections of 10(3) p.f.u. of each virus. Two WEEV strains, McMillan (McM) and Imperial 181 (IMP), were the most divergent of the six in genome sequence; McM caused 100 % mortality by 5 days post-infection, whereas IMP caused no mortality. McM had significantly higher titres in the brain than IMP. Similar differences in virulence were observed when McM and IMP were administered by aerosol, intranasal or intravenous routes. McM was 100 % lethal with an MTD of 1.9 days when 10(3) p.f.u. of each virus was administered by intracerebral inoculation; in contrast, IMP caused no mortality. The presence of IMP in the brains after infection by different routes and the lack of observed mortality confirmed that IMP is neuroinvasive but not neurovirulent. Based on morbidity, mortality, MTD, severity of brain lesions, virus distribution patterns, routes of infection and differences in infection of cultured cells, McM and IMP were identified as high- and low-virulence isolates, respectively. |
Antigenic and genetic characteristics of swine-origin 2009 A(H1N1) influenza viruses circulating in humans
Garten RJ , Davis CT , Russell CA , Shu B , Lindstrom S , Balish A , Sessions WM , Xu X , Skepner E , Deyde V , Okomo-Adhiambo M , Gubareva L , Barnes J , Smith CB , Emery SL , Hillman MJ , Rivailler P , Smagala J , de Graaf M , Burke DF , Fouchier RA , Pappas C , Alpuche-Aranda CM , Lopez-Gatell H , Olivera H , Lopez I , Myers CA , Faix D , Blair PJ , Yu C , Keene KM , Dotson PD Jr , Boxrud D , Sambol AR , Abid SH , St George K , Bannerman T , Moore AL , Stringer DJ , Blevins P , Demmler-Harrison GJ , Ginsberg M , Kriner P , Waterman S , Smole S , Guevara HF , Belongia EA , Clark PA , Beatrice ST , Donis R , Katz J , Finelli L , Bridges CB , Shaw M , Jernigan DB , Uyeki TM , Smith DJ , Klimov AI , Cox NJ . Science 2009 325 (5937) 197-201 Since its identification in April 2009, an A(H1N1) virus containing a unique combination of gene segments from both North American and Eurasian swine lineages has continued to circulate in humans. The lack of similarity between the 2009 A(H1N1) virus and its nearest relatives indicates that its gene segments have been circulating undetected for an extended period. Its low genetic diversity suggests that the introduction into humans was a single event or multiple events of similar viruses. Molecular markers predictive of adaptation to humans are not currently present in 2009 A(H1N1) viruses, suggesting that previously unrecognized molecular determinants could be responsible for the transmission among humans. Antigenically the viruses are homogeneous and similar to North American swine A(H1N1) viruses but distinct from seasonal human A(H1N1). |
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